Abstract:
:Some tumor cell lines secrete high concentrations of TGFbeta or IL-1. Similarly high concentrations of each of these cytokines cross-activate the other pathway: TGFbeta activates NFkappaB, and IL-1beta activates Smads. The IL-1 signaling components IRAK, MyD88, TRAF6, and TAK1 are all required for cross-activation of NFkappaB by TGFbeta. Knockdown experiments revealed that both TGFbeta receptor subunits are required for IL-1beta to activate Smads, and the IL-1 receptor is required for TGFbeta to activate NFkappaB. Coimmunoprecipitations showed that either TGFbeta or IL-1beta stimulate ligand-dependent association of all three receptor subunits. Furthermore, cross-talk between the TGFbeta and IL-1 signaling pathways leads to dose-dependent cross-control of gene expression. These interactions provide new insight into biological responses to IL-1 and TGFbeta in the proximity of tumors that secrete high concentrations of these factors and probably also at sites of inflammation, where the local concentrations of these cytokines are likely to be high.
journal_name
Proc Natl Acad Sci U S Aauthors
Lu T,Tian L,Han Y,Vogelbaum M,Stark GRdoi
10.1073/pnas.0700118104subject
Has Abstractpub_date
2007-03-13 00:00:00pages
4365-70issue
11eissn
0027-8424issn
1091-6490pii
0700118104journal_volume
104pub_type
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